Erythroid cells are the major consumers of body iron. The continual turnover of red cells and the retention of iron by the body requires an iron storage and recycling system. In adult animals, iron is stored in ferritin and hemosiderin in the liver, spleen and marrow. Iron that is stored as ferritin in immature red cells within marrow is essentially consumed by the end of red cell maturation. If the iron storage capacity of the body is exceeded, toxic deposits of the excess iron form in the tissues. Early in the development of an animal, the primitive (larval or embryonic) red cells store iron in ferritin. In the bullfrog tadpole, for example, mature red cells contain large amounts of ferritin (1% of the soluble protein) which accounts for 30% of the red cell iron and approximately 35% of the body ferritin iron. Since exogenous iron controls the ferritin concentration in adult storage tissues such as liver, by regulating ferritin synthesis (translation of stored m-RNA) and degradation, it is proposed to analyze the regulation of ferritin concentration in primitive and definitive red cells under varying conditions of exogenous iron concentration and source (transferrin, plasma) and to examine developmental changes in transferrin and iron delivery to red cells. In addition, genotypic variations in primitive (embryonic) red cell ferritin concentrations will be sought. The results should provide basic information about the regulation and the role of red cell ferritin and iron storage during animal development and may suggest a means of activating iron storage in mature adult red cells, thereby enlarging the iron storage capacity and possibly ameliorating some of the difficulties of iron overload. The results should be important in understanding diseases which involve iron overload and/or altered red cell iron storage, e.g., idiopathic hemachromatosis, thalassemia, sideroblastic anemia and some cases of sickle cell anemia and leukemia.